During the last few years genetic research with bacteria has made significant progress, and ample evidence has accumulated to show that the heredi-tary mechanism operating in bacteria may be sim-ilar to that in higher organisms. It has been dem-onstrated that hereditary changes, comparable to mutations, occur in bacteria, and that these cover a range of types similar to those found in fungi, where genetic analysis is possible (1). Further-more, an association resembling linkage in higher organisms has been observed in bacteria (2). Experimental evidence indicates that changes in bacteria from sensitivity to resistance to penicillin and streptomycin originate as mutations, and that these antibiotics act only as selective agents which eliminate the sensitive bacteria and thus allow the resistant mutants, which are always present in any large population, to multiply (3). Experiments have revealed that the development of high re-sistance follows a definite pattern, which appears to be characteristic for each antibiotic and which is not determined by the bacteria involved. De-tailed analyses of the pattern of streptomycin re-sistance have been made by me 'With Escherichia coli and Staphylococcus aureus, and by Dr. V. Bryson (unpublished) with Mycobacterium ranae. This work has revealed a remarkable similarity of behavior in these species of bacteria. Quantita-tive studies of penicillin resistance have been made only with Staphylococcus aureus (4, 5), but the results of other investigators, who have studied various phases of the action of penicillin with a wide variety of species, do not suggest that the pat-tern of resistance to penicillin is different in other bacteria from that analyzed with Staphylococcus. At present two patterns of resistance have been established, the penicillin pattern and the strepto-mycin pattern. A "stepwise " development of re-
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M. Demerec (1949) studied this question.
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